Component

Forskolin

Forskolin. Species, exposure and limitations are retained in each linked claim.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others.

    Human cannabinoid receptor 1 / CB1 / CNR1 → Cellular cyclic AMP accumulation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"}
    experimental_model
    Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1
    exposure
    A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin
    limitations
    Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed.
    nutrient_topic
    THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
    organism
    Human receptor in CHO cells
    plain_language
    The same receptor can push cAMP up as well as down, and which way depends on which drug is bound.
    primary_references
    [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
    tissue_or_cell_type
    Transfected cells

    THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 179–190

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 · source_derived_draft · unverified_draft

    ### thc-agonist-specific-trafficking Cannabinoid receptors coupled to both Gs and Gi and could consequently stimulate or inhibit cAMP formation, with an identical rank order of agonist potency in both assays but markedly different intrinsic activities, anandamide and CP-55,940 being much less efficacious at stimulating cAMP than at inhibiting it, and forskolin enhancing the potency of some agonists a hundred-fold while not affecting others. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The same receptor can push cAMP up as well as down, and which way depends on which drug is bound. organism: Human receptor in CHO cells tissue_or_cell_type: Transfected cells experimental_model: Quantified potency and intrinsic activity of cannabinoid ligands on cAMP in CHO cells expressing human CB1 limitations: Reports that the receptor couples to Gs as well as Gi and that ligands differ between the two pathways. It is a transfected overexpression system, where Gs coupling is more readily observed. exposure: A ligand series measured for both stimulation and inhibition of cAMP, with and without forskolin evidence_span: {"source_cache": "artifacts/thc-research/9864268.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d", "start_char": 0, "end_char": 1502, "text_sha256": "a39487ffec2ec3efa585fd49076c7498e8db3bf0ab943fe267e431b93dc7483d"} [thc-p9864268] Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: evidence for agonist-specific trafficking of intracellular responses. (1998). https://pubmed.ncbi.nlm.nih.gov/9864268/ DOI: 10.1016/s0022-3565(24)37876-0
    Complete structured claim and evidence

  2. In Dio2-null brown adipocytes the acute norepinephrine-, CL316,243- or forskolin-induced increases in lipolysis, UCP1 mRNA and oxygen consumption were all reduced because of impaired cAMP generation, and all were completely reversed by a single T3 injection 14 hours earlier.

    Experimental Dio2-disrupted mouse genotype → Cyclic adenosine monophosphate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"}
    experimental_model
    Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue
    exposure
    Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection
    limitations
    The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Mouse
    plain_language
    Without locally made hormone the cell cannot even hear the nerve signal properly.
    primary_references
    [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    tissue_or_cell_type
    Brown adipose tissue
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 403–414

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue · source_derived_draft · unverified_draft

    ### cold-dio2-camp-defect In Dio2-null brown adipocytes the acute norepinephrine-, CL316,243- or forskolin-induced increases in lipolysis, UCP1 mRNA and oxygen consumption were all reduced because of impaired cAMP generation, and all were completely reversed by a single T3 injection 14 hours earlier. Condition category: nutrient_deficiency nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Without locally made hormone the cell cannot even hear the nerve signal properly. organism: Mouse tissue_or_cell_type: Brown adipose tissue experimental_model: Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue limitations: The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone. exposure: Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection evidence_span: {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"} [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    Complete structured claim and evidence

  3. Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle.

    Indicaxanthin → cAMP content in mouse ileal muscle source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract
    duration
    Acute responses; exact interval not in accessed abstract
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Isolated mouse ileal longitudinal muscle
    limitations
    PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Isolated mouse ileal longitudinal muscle
    plain_language
    Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle.
    primary_references
    Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034
    route
    Ex vivo organ-bath addition
    tissue
    Organ-bath smooth muscle

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 96–105

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Isolated mouse ileal longitudinal muscle · source_derived_draft · unverified_draft

    ## indicaxanthin-ileal-camp Adding indicaxanthin increased basal and forskolin-stimulated cAMP in mouse ileal muscle. Model/species: Isolated mouse ileal longitudinal muscle Tissue: Organ-bath smooth muscle Exposure: Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract Route: Ex vivo organ-bath addition Duration: Acute responses; exact interval not in accessed abstract Limits: PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested. Primary reference: Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034 Access: Primary PubMed abstract.
    Complete structured claim and evidence

  4. Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity.

    Indicaxanthin → Forskolin-induced inhibition of mouse ileal contractility source_derived_draftungraded
    Experimental context and source evidence
    dose
    Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract
    duration
    Acute responses; exact interval not in accessed abstract
    evidence_access
    Primary PubMed abstract.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Isolated mouse ileal longitudinal muscle
    limitations
    PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested.
    nutrient_topic
    Dedicated indicaxanthin chapter; original betalain family identity and shared claims preserved. · Indicaxanthin
    organism
    Isolated mouse ileal longitudinal muscle
    plain_language
    Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity.
    primary_references
    Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034
    route
    Ex vivo organ-bath addition
    tissue
    Organ-bath smooth muscle

    Indicaxanthin: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 107–116

    Original AI-assisted curation of thirteen additional primary studies, with twenty-six existing claims from eight studies linked unchanged. Study-specific citations and limitations retained. Not publisher full text. · supports · Isolated mouse ileal longitudinal muscle · source_derived_draft · unverified_draft

    ## indicaxanthin-ileal-forskolin Indicaxanthin enhanced the inhibitory effect of forskolin on mouse ileal mechanical activity. Model/species: Isolated mouse ileal longitudinal muscle Tissue: Organ-bath smooth muscle Exposure: Indicaxanthin; forskolin, IBMX and other pharmacological probes, exact concentrations not in accessed abstract Route: Ex vivo organ-bath addition Duration: Acute responses; exact interval not in accessed abstract Limits: PDE involvement is inferred pharmacologically, not established by an isoform-specific binding or purified-enzyme assay; no clinical motility treatment is tested. Primary reference: Inhibitory effects of indicaxanthin on mouse ileal contractility: analysis of the mechanism of action. (2011). https://pubmed.ncbi.nlm.nih.gov/21371457/ DOI: 10.1016/j.ejphar.2011.02.034 Access: Primary PubMed abstract.
    Complete structured claim and evidence

  5. 6-Gingerol pretreatment increased the forskolin-stimulated intracellular cAMP response in human neutrophils.

    6-Gingerol → Intracellular cAMP in human neutrophils source_derived_draftungraded
    Experimental context and source evidence
    dose
    6-Gingerol 10 micromolar followed by forskolin 100 micromolar
    duration
    30 min gingerol followed by 10 min forskolin
    evidence_access
    Primary open full text, results, figure legends and methods, plus PubMed metadata.
    evidence_scope
    literature_reviewed; model-specific source-derived curation, not universally established human effects
    experimental_model
    Neutrophils isolated from healthy human donors
    limitations
    Potentiation of a forskolin-stimulated signal is not proof of the same magnitude under basal conditions.
    nutrient_topic
    Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
    organism
    Neutrophils isolated from healthy human donors
    plain_language
    6-Gingerol pretreatment increased the forskolin-stimulated intracellular cAMP response in human neutrophils.
    primary_references
    Antineutrophil properties of natural gingerols in models of lupus. (2021). https://pubmed.ncbi.nlm.nih.gov/33373329/ DOI: 10.1172/jci.insight.138385
    route
    Ex vivo exposure
    tissue
    Human neutrophil cytosol

    Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 459–468

    Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Neutrophils isolated from healthy human donors · source_derived_draft · unverified_draft

    ## gingerols-6-neutrophil-camp 6-Gingerol pretreatment increased the forskolin-stimulated intracellular cAMP response in human neutrophils. Model/species: Neutrophils isolated from healthy human donors Tissue: Human neutrophil cytosol Exposure: 6-Gingerol 10 micromolar followed by forskolin 100 micromolar Route: Ex vivo exposure Duration: 30 min gingerol followed by 10 min forskolin Limits: Potentiation of a forskolin-stimulated signal is not proof of the same magnitude under basal conditions. Primary reference: Antineutrophil properties of natural gingerols in models of lupus. (2021). https://pubmed.ncbi.nlm.nih.gov/33373329/ DOI: 10.1172/jci.insight.138385 Access: Primary open full text, results, figure legends and methods, plus PubMed metadata.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards